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PubMed1978

Index for the assessment of heat tolerance.

Heat tolerance was assessed by magnitude of strain induced in the body as a whole by heat load. The strain was represented by a combination of relative water loss, relative rise in rectal temperature and relative salt loss, using those critical values of the three factors which cause heat stroke (40.6 degrees C), water depletion heat exhaustion (7% of body weight) and salt depletion heat exhaustion (0.75 g per kg of body weight). As this numerical heat tolerance index is defined as the degree of disturbance induced by heat exposure concerning thermal regulation, water and electrolyte metabolism, the magnitude of the index is inversely proportional to that of heat tolerance. Our studies showed that adaptive changes in heat tolerance of unacclimatized subjects during short-term heat acclimatization could be followed up by this heat tolerance index and that superior heat tolerance of residents in subtropical zone and athletes could by reasonably evaluated by the index. Thus, it might be said that this numerical heat tolerance index is a reliable index for the assessment of heat tolerance.

Acclimatization↗
PubMed1984

Heat Stress Responses in Cultured Plant Cells : Heat Tolerance Induced by Heat Shock versus Elevated Growing Temperature.

Using cultured pear (Pyrus communis cv Bartlett) cells, heat tolerance induced by heat shock was compared to that developed during growth at high temperature. After growth at 22 degrees C, cells exposed to 38 degrees C for 20 minutes (heat shock) showed maximum increased tolerance within 6 hours. Cells grown at 30 degrees C developed maximum heat tolerance after 5 to 6 days; this maximum was well below that induced by heat shock. Heat shock-induced tolerance was fully retained at 22 degrees C for 2 days and was only partly lost after 4 days. However, pear cells acclimated at 30 degrees C lost all acquired heat tolerance 1 to 2 days after transfer to 22 degrees C. In addition, cells which had been heat-acclimated by growth at 30 degrees C showed an additional increase in heat tolerance in response to 39 degrees C heat shock. The most striking difference between heat shock and high growth temperature effects on heat tolerance was revealed when tolerance was determined using viability tests based on different cell functions. Growth at 30 degrees C produced a general hardening, i.e. increased heat tolerance was observed with all three viability tests. In contrast, significantly increased tolerance of heat-shocked cells was observed only with the culture regrowth test. The two types of treatment evoke different mechanisms of heat acclimation.

Journal Article↗
PubMed1979

Studies on heat tolerance at rest and orthostatic heat tolerance in a hot environment.

Twelve young male Japanese were exposed to a hot environment in summer, and changes in systolic blood pressure induced by changing the position from recumbent to sitting were observed. Sweating was induced in a climatic chamber at 30 degree C with 70% relative humidity by immersing both legs up to the knees into a water bath of 42 degree C for 90 min after sitting on a chair at rest for 30 min in the chamber. The mean values of rise in rectal temperature, body weight loss and mean sodium concentration in sweat were 0.62 degree C, 0.67 kg and 46 mEq/l, respectively. The mean values of fall in systolic blood pressure associated with changing posture and its recovery time were 13.7 mm Hg and 77.5 sec, respectively. Heat tolerance at rest was assessed by a numerical heat tolerance index involving relative water loss, relative rise in rectal temperature, and relative salt loss. Values of relative water loss, relative rise in rectal temperature, and the numerical heat tolerance index correlated closely to those of fall in systolic blood pressure and its recovery time.

Adult↗
PubMed1987

Isoproterenol sensitivity in heat tolerant and relatively heat intolerant men.

Recent research has demonstrated that pharmacologic blockade of beta-adrenoceptors predisposes to hyperthermia during prolonged exercise. To investigate the hypothesis that beta-adrenoceptor sensitivity to catecholamines may be an important determinant of exertional heat tolerance, we performed a cross-sectional study comparing the heart rate responses to graded doses of isoproterenol in 6 heat tolerant and 6 relatively heat intolerant men. We observed no significant difference (p greater than 0.1) between the heat tolerant (0.9 +/- 0.68 microgram) and heat intolerant (1.19 +/- 0.61 microgram) subjects in the dose of isoproterenol that produced a 25 beat.min-1 increment in heart rate. Although the possibility of a relationship between beta-adrenoceptor sensitivity and the ability to tolerate exercise in heat cannot be entirely excluded on the basis of these data, our study clearly demonstrates the lack of a correlation between cardiac pacemaker sensitivity to isoproterenol and exertional heat tolerance.

Adolescent↗
PubMedDate not supplied

Molecular genetics of heat tolerance and heat shock proteins in cereals.

Heat stress is common in most cereal-growing areas of the world. In this paper, we summarize the current knowledge on the molecular and genetic basis of thermotolerance in vegetative and reproductive tissues of cereals. Significance of heat stress response and expression of heat shock proteins (HSPs) in thermotolerance of cereal yield and quality is discussed. Major avenues for increasing thermotolerance in cereals via conventional breeding or genetic modification are outlined.

Adaptation, Physiological↗
PubMed2004

Assessment of heat tolerance for post exertional heat stroke individuals.

BACKGROUND: The aim of this study was to evaluate the heat tolerance test, which was performed by individuals with high risk for heat injuries, for exposure duration and climatic conditions. MATERIAL/METHODS: Nineteen young (19+/-1 yr) post heat stroke males performed 2 separate tolerance tests consisting of identical treadmill walking (5km.h-1, 2% grade) for 120 min during hot (40 degrees C, 40%RH) and comfort (20 degrees C, 50%RH) climate conditions. Physiological monitoring included rectal temperature (Tre), heart rate (HR), skin temperature and sweat rate (msw). Concomitantly, strain evaluation was assessed by the physiological strain index (PSI) and the cumulative heat strain index (CHSI). RESULTS: 14 subjects were categorized as heat tolerant (HT) and 5 subjects as heat intolerant (HI). The comfort tolerance test was found as irrelevant for heat intolerance assessment. PSI after 60 min (PSI60) was unable to predict PSI after 120 min (PSI120) whereas there was not a high enough correlation between CHSI60 and CHSI120. CONCLUSIONS: It was concluded that tolerance to heat must be tested during heat stress and the test duration cannot be shorter than 120 min.

Adult↗
PubMed2001

Effects of calcium on antioxidant activities and water relations associated with heat tolerance in two cool-season grasses.

Calcium (Ca2+) may be involved in plant tolerance to heat stress by regulating antioxidant metabolism or/and water relations. This study was designed to examine whether external Ca2+ treatment would improve heat tolerance in two C(3), cool-season grass species, tall fescue (Festuca arundinacea L.) and Kentucky bluegrass (Poa pratensis L.), and to determine the physiological mechanisms of Ca2+ effects on grass tolerance to heat stress. Grasses were treated with CaCl(2) (10 mM) or H(2)O by foliar application and then exposed to heat stress (35/30 degrees C) in growth chambers. Some of the Ca2+ -untreated plants were maintained at 20/15 degrees C as the temperature control. Heat stress reduced grass quality, relative water content (RWC), and chlorophyll (Chl) content of leaves in both species, but Ca2+ treatment increased all three factors under heat stress. The Ca2+ concentration in cell saps increased with heat stress and with external Ca2+ treatment in both species. Osmotic potential increased with heat stress, but external Ca2+ treatment had no effect. Osmotic adjustment increased during short-term heat stress, but then decreased with a prolonged period of stress; it was not influenced by Ca2+ treatment. The activity of superoxide dismutase (SOD) in both species increased transiently at 12 d of heat stress and then remained at a level similar to that of the control. External Ca2+ treatment had no effect on SOD activity. The activities of catalase (CAT), ascorbate peroxidase (AP), and glutathione reductase (GR) of both species decreased during heat stress. Plants treated with Ca2+ under heat stress had higher CAT, GR and AP activities than untreated plants. Lesser amounts of malondialdehyde (MDA) accumulated in Ca2+ -treated plants than in untreated plants during extended periods of heat stress. The results suggested that exogenous Ca2+ treatment enhanced heat tolerance in both tall fescue and Kentucky bluegrass. This enhancement was related to the maintenance of antioxidant activities and a decrease in membrane lipid peroxidation, but not to the regulation of osmotic potential and osmotic adjustment.

Antioxidants↗
PubMed2003

Regulation mode of evaporative cooling underlying a strategy of the heat-tolerant FOK rat for enduring ambient heat.

Compared with other rat strains, the inbred FOK rat is extremely heat tolerant. This increased heat tolerance is due largely to the animal's enhanced saliva spreading abilities. The aims of the present study were to 1) quantify the heat tolerance capacity of FOK rats and 2) determine the regulatory mode of the enhanced salivary cooling in these animals. Various strains of rats were acutely exposed to heat. In the heat-intolerant strains, saliva spreading was insufficient and the core temperature (Tc) rose rapidly. In contrast, FOK rats maintained an elevated Tc plateau (39.5 +/- 0.7 degrees C) for 5-6 h over a wide range of ambient temperatures (Ta) (37.5-42.5 degrees C). In hot environments the FOK rats secreted copious amounts of saliva and spread it over more than the entire ventral body surface. FOK rats had a low Tc threshold for salivation, and the salivation rate increased linearly in proportion to the Tc deviation from the threshold. No strain difference or temperature effect was observed in the saliva secretion rate from in vitro submandibular glands perfused by sufficient doses of ACh. These results suggest that 1) the ability of FOK rats to maintain a moderate steady-state hyperthermia (39.5 +/- 0.7 degrees C) over a wide Ta range is enabled by a lowered threshold Tc for salivation and functional negative-feedback control of saliva secretion and 2) strain differences in ability to endure heat stress are mainly attributable to changes in the thermoregulatory control system rather than altered secretory abilities of the salivary glands.

Adaptation, Physiological↗
PubMed2006

Pre-existing inflammatory state compromises heat tolerance in rats exposed to heat stress.

This study investigated the roles of endotoxemia and heat-induced tissue damage in the pathology of heat stroke. In groups of eight, male Wistar rats were treated with heat exposure only (HE), or heat exposure with turpentine (T+HE), dexamethasone (D+HE), and turpentine and dexamethasone combined (TD+HE). The rats remained sedated for 2 h after receiving the respective treatments, followed by heat exposure until the core temperature (T(c)) was 42 degrees C for 15 min; control rats received turpentine (T), dexamethasone (D), and turpentine and dexamethasone (TD) without heat stress. Blood samples were collected before treatment (baseline I), after 2 h of passive rest (baseline II), at T(c) 40 degrees C (T40), and 15 min after achieving T(c) 42 degrees C (T42). No rats died in the nonheat-stressed groups. Survival rate was lowest in the TD+HE rats (37.5%), followed by the HE (62.5%), T+HE (75%), and D+HE (100%) rats (P < 0.05). The duration of survival at T42 degrees C was shortest in the TD+HE rats (9.9 +/- 6.2 min) (P < 0.01), followed by the T+HE (11.3 +/- 6.1 min) and the HE (12.2 +/- 4 min) (P < 0.05) rats. The increase in plasma IL-6 concentrations was highest in the T+HE (352%) and HE (178%) rats (P < 0.05). D+HE treatment suppressed the increases in plasma aspartate transaminase, alanine aminotransferase, and IL-6 and LPS concentrations during severe heat stress. Heat stroke can be triggered by endotoxemia or heat-induced tissue damage, and preexisting inflammation compromises heat tolerance, whereas blocking endotoxemia increases heat tolerance.

Alanine Transaminase↗
PubMed2005

The impact of rosiglitazone on heat tolerance in patients with type 2 diabetes.

BACKGROUND: Diabetes is associated with reduced tolerance to heat. The insulin sensitizer rosiglitazone (RSG), administered for glycemic control, has a secondary effect in increasing vascular endothelial function. The hypothesis to be tested was if administration of rosiglitazone would increase heat tolerance in people with diabetes. MATERIAL/METHODS: Thirty subjects with diabetes and thirty control subjects were examined. A subset of 21 subjects with diabetes had RSG administered at 4 mg per day for a period of 1 year. At 2 weeks, 4 weeks, 3 months, 6 months, and 1 year post administration, measurements were taken to assess any potential impact of this drug on thermoregulation. Parameters measured were sweat rate, skin temperature, body core temperature, and skin blood flow. RESULTS: Results of these experiments showed that subjects with diabetes at baseline had 1) sensory impairment, 2) sweat gland impairment 3) high skin temperatures, 4) and low blood flow reduction during heat exposure, all leading to higher core temperature compared to controls subjects. After administration of rosiglitazone for 1 year significant improvements in thermoregulation were observed. Trends for improvement in thermoregulation were observed close to that of age matched control subjects. CONCLUSIONS: Heat tolerance can be improved in people with diabetes when taking the insulin sensitizer RSG for Glycemic control, probably due to increased endothelial cell function.

Aged↗
PubMed1989

Improvements in heat tolerance induced by interval running training in the heat and in sweat clothing in cool conditions.

To compare the effectiveness of training in heat and in sweat clothing in cool conditions on improving heat tolerance, two groups of active subjects (n = 6 in each) performed an interval running heat-tolerance test before and after a 7-day experimental treatment. On each treatment day the subjects attempted to complete 4 x 15 min interval treadmill running periods (a 7.5 s effort every 30 s, on 15 km h-1, 15% grade; the same exercise format as the heat-tolerance test), which were interspersed with 5-min recovery periods (total time each day = 80 min). Group 1 (heat) ran in shorts, socks and shoes in hot humid conditions, and Group 2 (sweat clothing) ran in cool conditions dressed in shorts, socks and T-shirt covered by a polyester-cotton tracksuit, over which was worn 100% nylon spray-proof pants and jacket (cotton lined) with an acrylic cloth bobble hat (beanie) on the head. Both groups displayed changes typical of heat acclimatization over the 7-day period, with significant decreases in final rectal temperature (Tr) and heart rate (HR) being evident, but no change in sweat loss. Mean skin temperature (Tsk) was similar in both groups during the training sessions (heat group: 34.8-35.7 degrees C; sweat clothing group 34.9-35.5 degrees C). After the heat-tolerance test, both groups had significantly lower Tr, Tsk and HR values than before, and sweating sensitivity (g m-2 h-1 degrees C rise in Tr) was significantly increased. There was only one significant difference between the two groups (Tsk, 20th min value). It was concluded that training in sweat clothing in cool conditions can provide the same improvements in heat tolerance as training in hot humid conditions where a fixed exercise intensity and duration are used.

Acclimatization↗
PubMedDate not supplied

Aging and human heat tolerance.

Collectively, the literature on heat tolerance suggests that middle-aged (45- to 64-year-old) men and women are more work-heat-intolerant and suffer more physiological strain during heat acclimation than younger individuals. However, it is unclear whether the age differences in work-heat intolerance and physiological strain during heat acclimation are related to age per se or associated with other factors such as certain disease states, decreased physical activity, or lowered aerobic fitness. In contrast, the work-heat tolerance and physiological responses during heat acclimation of habitually active or aerobically trained middle-aged men are the same as or better than younger individuals. The reviewed studies emphasize the importance of aerobic fitness and pertinent morphological factors, such as body fat, body weight, and surface area in maintaining work-heat tolerance with aging. Recent studies suggest that middle-aged and older men and women may be more susceptible to greater heat strain at physiologically significant levels of dehydration than those younger. However, additional research appears necessary to support this hypothesis. When the effects of chronic debilitating diseases in the elderly (64 years old and older) are minimized, their heat tolerance and thermoregulatory responses are comparable to those of younger individuals. In fact, healthy and well acclimated elderly men and women appear to perform as well as younger individuals during desert walks in dry heat. This review discusses experimental observations from previously published studies concerning aging and heat tolerance or the physiological heat strain during heat acclimation at rest or during work; and it suggests future research efforts needed to understand this topic better.

Aging↗
PubMed1994

Abscisic acid-induced heat tolerance in Bromus inermis Leyss cell-suspension cultures. Heat-stable, abscisic acid-responsive polypeptides in combination with sucrose confer enhanced thermostability.

Increased heat tolerance is most often associated with the synthesis of heat-shock proteins following pre-exposure to a nonlethal heat treatment. In this study, a bromegrass (Bromus inermis Leyss cv Manchar) cell suspension cultured in a medium containing 75 microM abscisic acid (ABA) without prior heat treatment had a 87% survival rate, as determined by regrowth analysis, following exposure to 42.5 degrees C for 120 min. In contrast, less than 1% of the control cells survived this heat treatment. The heat tolerance provided by treatment with 75 microM ABA was first evidenced after 4 d of culture and reached a maximum tolerance after 11 d of culture. Preincubation with sucrose partially increased the heat tolerance of control cells and rendered ABA-treated cells tolerant to 45 degrees C for 120 min (a completely lethal heat treatment for control cells). Comparative two-dimensional polyacrylamide gel electrophoresis of cellular protein isolated from heat-tolerant cells identified 43 ABA-responsive proteins of which 26 were heat stable (did not coagulate and remained soluble after 30 min at 90 degrees C). Eight heat-stable, ABA-responsive proteins ranging from 23 to 45 kD had similar N-terminal sequences. The ABA-responsive (43-20 kD), but none of the control heat-stable, proteins cross-reacted to varying degrees with a polyclonal antibody directed against a conserved, lysine-rich dehydrin sequence. A group of 20- to 30-kD heat-stable, ABA-responsive proteins cross-reacted with both the anti-dehydrin antibody and an antibody directed against a cold-responsive winter wheat protein (Wcs 120). In ABA-treated cells, there was a positive correlation between heat- and pH-induced coagulation of a cell-free homogenate and the heat tolerance of these cells. At 50 degrees C, control homogenates coagulated after 8 min, whereas cellular fractions from ABA-treated cells showed only marginal coagulation after 15 min. In protection assays, addition of heat-stable, ABA-responsive polypeptides to control fractions reduced the heat-induced coagulation of cell-free homogenates. Sucrose (8%) alone and control, heat-stable fractions enhanced the thermostability of control fractions, but the most protection was conferred by ABA-responsive, heat-stable proteins in combination with sucrose. These data suggest that stress-tolerance mechanisms may develop as a result of cooperative interactions between stress proteins and cell osmolytes, e.g. sucrose. Hypotheses are discussed implicating the role of these proteins and osmolytes in preventing coagulation and denaturation of cellular proteins and membranes.

Abscisic Acid↗
PubMed2003

Effect of hyperglycemia and nitric oxide synthase inhibition on heat tolerance and induction of heat shock protein 72 kDa in vivo.

Diabetes and nitric oxide synthase (NOS) inhibition both exacerbate mesenteric ischemia/ reperfusion injury. Heat shock protein 72 (HSP-72) protects against KDa ischemia/reperfusion damage in vivo. The effect of diabetes on HSP-72 expression in vivo is unknown. The aim of this study was to determine the effects of diabetes and NOS inhibition on HSP-72 induction in vivo. Rats were assigned to four groups: control (C), streptozotocin-induced diabetic (D), acute hyperglycemia (A), and L-N(omega)-nitro-L-arginine treated (L). Rats were subjected to hyperthermia and allowed to recover for 4 hours. Intestine and liver samples from heated (H) and nonheated (NH) rats were analyzed for HSP-72 by Western blot. HSP-72 levels were increased significantly in CH compared to CNH rats. No deaths occurred in CH rats; however, death rates were significant in AH, DH, and LH rats. DH rats died earlier than LH and AH rats. HSP-72 in liver and intestine was reduced significantly in LH rats. When compared with CH rats the surviving AH and DH rats exhibited similar HSP-72 levels in the liver. Diabetes, acute hyperglycemia, and L-N(omega)-nitro-L-arginine treatment lower heat stress tolerance. NOS is required for HSP-72 expression, but not survival. Diabetics who survive heat stress moderately express HSP-72. Characterization of altered thermotolerance and HSP-72 may provide mechanisms for the deranged diabetic stress response.

Acute Disease↗
PubMed1987

Evaluation of a temperate environment test to predict heat tolerance.

A temperate environment heat tolerance test (HTT) was formerly reported (Shvartz et al. 1977b) to distinguish heat acclimatized humans from former heat stroke patients. The purpose of this investigation was to evaluate the ability of HTT to measure acute individual changes in the HR and Tre responses of normal subjects, induced by classical heat acclimation procedures, thereby assessing the utility and sensitivity of HTT as a heat tolerance screening procedure. On day 1, 14 healthy males performed HTT (23.2 +/- 0.5 degrees C db, 14.9 +/- 0.5 degrees C wb) by bench stepping (30 cm high, 27 steps x min-1) for 15 min at 67 +/- 3% VO2max. On days 2-9, all subjects underwent heat acclimation (41.2 +/- 0.3 degrees C db, 28.4 +/- 0.3 degrees C wb) via treadmill exercise. Heat acclimation trials (identical on days 2 and 9) resulted in significant decreases in HR (170 +/- 3 vs 144 +/- 5 beats x min-1), Tre (39.21 +/- 0.09 vs 38.56 +/- 0.17 degrees C), and ratings of perceived exertion; plasma volume expanded 5.2 +/- 1.7%. On day 10, subjects repeated HTT; day 1 vs day 10 HR were statistically similar (143 +/- 6 vs 137 +/- 6 beats x min-1, p greater than 0.05) but Tre decreased significantly (37.7 +/- 0.1 vs 37.5 +/- 0.1 degrees C, p less than 0.05). Group mean HTT composite score (day 1 vs day 10) was unchanged (63 +/- 5 vs 72 +/- 6, p greater than 0.05), and individual composite scores indicated that HTT did not accurately measure HR and Tre trends at 41.2 +/- degrees C in 6 out of 14 subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Acclimatization↗
PubMed2006

[Cloning of GmHSFA1 gene and its overexpression leading to enhancement of heat tolerance in transgenic soybean].

Heat shock transcription factors (HSFs) are important in regulating heat stress response by mediating expression of heat shock protein (HSP) genes in various plant species. In the present study, a novel GmHSFA1 with an ORF of 1,533 bp (full-length cDNA sequence of 1,781 bp) was cloned from soybean genome via comparative genomic approach and RACE (rapid amplification of cDNA ends). This gene encodes 510 amino acids consisting of a protein of 56.2 kDa (GenBank accession number: AY458843). Similar to other HSFs, GmHSFA1 has the basic modular structure including DBD, OD, NLS, and CTAD. BLAST analysis revealed the identity of 52.46% between amino acid sequences between GmHSFA1 and LpHSFA1 that has the highest similarity to GmHSFA1 in all HSFA1s in various plant species. The results from RT-PCR, Northern blotting, and transformation showed: 1) GmHsfA1 exhibited the constitutive expression patterns in different tissues of soybean; 2) The expression level of GmHsfA1 in transgenic plants was notably higher than that in non-transgenic plants; 3) Overexpression of GmHsfA1 activated transcription of GmHSP22 in transgenic plants under normal conditions and enhanced obviously expressions of GmHSP23 and GmHSP70 in transgenic plants under heat stress conditions; 4) Heat tolerant temperature (as high as 52 degrees C) of transgenic plants was remarkably higher than that of non-transgenic plants. These results preliminarily proved that the overexpression of GmHsfA1 possibly led to the notable enhancement of heat-tolerant level of transgenic plants by mediating the activation of transcription or improvement of expression of some GmHSPs in the GmHsfA1's downstream in transgenic plants, suggesting GmHSFA1 is a novel and functional heat shock transcription factor of soybean.

Amino Acid Sequence↗
PubMed1995

Physical performance and heat tolerance after chronic water loading and heat acclimation.

Heat acclimation (HA) and forced water intake (FWI) have both been found to improve the endurance of human subjects working in hot environments. Therefore, we studied the interaction between HA and FWI. Prior to any treatment (control, AI and BI) the subjects (n = 9) underwent a heat tolerance (HT) test. Thereafter, they were divided into two groups. The first (n = 5) were heat-acclimated (AII), underwent a second HT test, doubled their normal daily water intake for 1 week (AIII), and underwent a third HT test; the second group (n = 4) were subjected to the same protocol, except that the FWI came before and during HA (BII). It was found that both regimens (phases AII and BII) significantly increased work duration. Although the results of the two methods were similar, their combination somewhat lengthened work tolerance time (phases AIII, BIII). Maximal oxygen uptake did not change after HA (BII) or FWI (AII), but the maximal values were attained at significantly lower heart rates, both after BII alone or combined with HA (BIII). In an additional experiment, the time needed to "ride" 15 km on a bicycle ergometer was reduced by 10% after FWI as compared to control time.

Acclimatization↗